Migraine headaches are the most severe or intensive type of headaches and affect approximately fifteen percent of the population. This disdorder is highly disruptive of the life of a sufferer thereof and also results in a very significant amount of lost work time. Moreover, there has been no really effective way to prevent the onset of such migraine headaches.
After the prodromal stage, the migraine attack has two main phases, namely the aural phase and the acute painful headache phase. Several symptons occur during the aural phase, such as visual scotomata (absence of vision within the visual field), spots, scintillating (flashing) visual scotomata, and other visual disturbances. Additionally, the migraine sufferer may become tired and possibly faint. As these symptoms of the aural phase slowly disappear, a throbbing hemi-cranial pain develops, either on one side, the front or the rear of the head. Other symptoms such as nausea or diarrhea may occur during a severe migraine headache. Migraine headaches develop suddenly and reach an intense level quickly.
Heretofore, a wide variety of pharmacological agents have been employed in attempts to treat a person suf fering from migraine headaches. For the most part, these pharmacological agents have been employed to treat the symptoms of a migraine headache after the onset or occurrence of the acute painful headache phase. Among the many types of pharmacological agents suggested for treatment of migraine headaches are antihistamines in combination with analgesics, vasodialators such as papaverine, beta-andrenergic blockers such as propranolol, nadolol, timolol and antenolol, calcium channel antagonists, and various phenothiazines.
Extracranial vasoconstrictors, such as ergot alkaloids, for example, ergotamine and sumatriptan, have also been employed since it has been considered that increased levels of norepinephrine, seratonin, bradykinin and substance P were considered to be the endogenous pain-producing compounds in combination with stretching due to vasoconstriction and vasodilation resulting as a reflex action to a variety of stimuli, such as intense light, noise, anxiety, exertion, cold, heat, hormones, and certain foods.
Recently in U.S. Pat. No. 5,250,529 it is suggested to treat migraine patients with a mast cell degranulation blocking agent, e.g. hydroxyzine or ketotifen, alone or in combination with a central nervous system stimulant, e.g. caffeine, just prior to or during the prodomol stage of the migraine so as to inhibit the release from mast cells of the vasoactive and nociceptive compounds involved in precipitating the migraine headache. This treatment is proposed based on the assumption that increased levels of norepinephrine, serotonin, bradykinin and substance P, as well as products of tissue anoxia are considered to be the endogenous pain-producing compounds. However, even this suggested treatment has not led to a successful means to prevent development of a migraine headache.
It is therefor an object of this invention to provide a method of preventing and alleviating migraine headaches in patients subject to such migraine headaches, and to compositions or dietary regimens to accomplish same.